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肥胖症:基因、大脑、肠道和环境。

Obesity: genes, brain, gut, and environment.

机构信息

UND Life Sciences, Shaker Heights, Ohio, USA.

出版信息

Nutrition. 2010 May;26(5):459-73. doi: 10.1016/j.nut.2009.09.020. Epub 2009 Dec 22.

DOI:10.1016/j.nut.2009.09.020
PMID:20022465
Abstract

Obesity, which is assuming alarming proportions, has been attributed to genetic factors, hypothalamic dysfunction, and intestinal gut bacteria and an increase in the consumption of energy-dense food. Obesity predisposes to the development of type 2 diabetes mellitus, hypertension, coronary heart disease, and certain forms of cancer. Recent studies have shown that the intestinal bacteria in obese humans and mice differ from those in lean that could trigger a low-grade systemic inflammation. Consumption of a calorie-dense diet that initiates and perpetuates obesity could be due to failure of homeostatic mechanisms that regulate appetite, food consumption, and energy balance. Hypothalamic factors that regulate energy needs of the body, control appetite and satiety, and gut bacteria that participate in food digestion play a critical role in the onset of obesity. Incretins, cholecystokinin, brain-derived neurotrophic factor, leptin, long-chain fatty acid coenzyme A, endocannabinoids and vagal neurotransmitter acetylcholine play a role in the regulation of energy intake, glucose homeostasis, insulin secretion, and pathobiology of obesity and type 2 diabetes mellitus. Thus, there is a cross-talk among the gut, liver, pancreas, adipose tissue, and hypothalamus. Based on these evidences, it is clear that management of obesity needs a multifactorial approach.

摘要

肥胖症的比例正在迅速上升,其病因可归结为遗传因素、下丘脑功能障碍、肠道细菌以及高热量食物摄入的增加。肥胖症容易导致 2 型糖尿病、高血压、冠心病和某些类型的癌症。最近的研究表明,肥胖人群和肥胖小鼠的肠道细菌与瘦人群体的肠道细菌不同,这可能引发低度全身炎症。高热量饮食引发并持续导致肥胖的原因可能是调节食欲、食物摄入和能量平衡的体内平衡机制出现故障。调节身体能量需求、控制食欲和饱腹感的下丘脑因子,以及参与食物消化的肠道细菌,在肥胖的发生中起着关键作用。肠促胰岛素、胆囊收缩素、脑源性神经营养因子、瘦素、长链脂肪酸辅酶 A、内源性大麻素和迷走神经递质乙酰胆碱在调节能量摄入、葡萄糖稳态、胰岛素分泌以及肥胖和 2 型糖尿病的病理生理学中发挥作用。因此,肠道、肝脏、胰腺、脂肪组织和下丘脑之间存在相互作用。基于这些证据,很明显,肥胖症的管理需要采取多因素方法。

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